BACKGROUND: Cholestasis has been identified as a risk factor for oxidative stress, and it potentially enhances after ischemic-reperfusion injury. The aim of this study was to evaluate the role of methylprednisolone on warm ischemia-reperfusion injury in the presence of cholestasis. METHODS: A reversible cholestatic rat model was created. After 7 days, rats received 30 mg/kg of intravenous methylprednisolone 2 hours before ischemia, followed by 30 minutes of ischemia. Rats were euthanized 24 hours after ischemia. Serum aspartate aminotransferase and interleukin-6 were measured, and the liver was harvested for histology and myeloperoxidase estimation. RESULTS: Methylprednisolone had a protective effect, with a statistically significant decrease in aspartate aminotransferase (P=.01) and a trend toward decreased levels of interleukin-6 (P=.07). Histology showed a significant difference in architectural distortion (P=.01), cytoplasmic vacuolation (P=.01), and nodular hepatocellular necrosis (P=.04). CONCLUSIONS: Methylprednisolone attenuated the ischemic-reperfusion injury in the presence of cholestasis and can be considered for clinical use in the presence of cholestasis. Copyright (c) 2010 Elsevier Inc. All rights reserved.
BACKGROUND:Cholestasis has been identified as a risk factor for oxidative stress, and it potentially enhances after ischemic-reperfusion injury. The aim of this study was to evaluate the role of methylprednisolone on warm ischemia-reperfusion injury in the presence of cholestasis. METHODS: A reversible cholestaticrat model was created. After 7 days, rats received 30 mg/kg of intravenous methylprednisolone 2 hours before ischemia, followed by 30 minutes of ischemia. Rats were euthanized 24 hours after ischemia. Serum aspartate aminotransferase and interleukin-6 were measured, and the liver was harvested for histology and myeloperoxidase estimation. RESULTS:Methylprednisolone had a protective effect, with a statistically significant decrease in aspartate aminotransferase (P=.01) and a trend toward decreased levels of interleukin-6 (P=.07). Histology showed a significant difference in architectural distortion (P=.01), cytoplasmic vacuolation (P=.01), and nodular hepatocellular necrosis (P=.04). CONCLUSIONS:Methylprednisolone attenuated the ischemic-reperfusion injury in the presence of cholestasis and can be considered for clinical use in the presence of cholestasis. Copyright (c) 2010 Elsevier Inc. All rights reserved.
Authors: Shoichi Kageyama; Kojiro Nakamura; Takehiro Fujii; Bibo Ke; Rebecca A Sosa; Elaine F Reed; Nakul Datta; Ali Zarrinpar; Ronald W Busuttil; Jerzy W Kupiec-Weglinski Journal: Hepatology Date: 2018-05-10 Impact factor: 17.425